Postjunctional α2-adrenoceptors are not present in proximal arterioles of rat intestine

1998 ◽  
Vol 274 (1) ◽  
pp. H202-H208 ◽  
Author(s):  
Geoffrey P. Nase ◽  
Matthew A. Boegehold
Keyword(s):  
Shear Stress ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Receptor Activation ◽  
Sympathetic Nerve Stimulation ◽  
No Release ◽  
Before And After ◽  
Sympathetic Nerve Activation ◽  
Intestinal Submucosa ◽  
Resting Tone

The purpose of this study was to evaluate two potential stimuli for nitric oxide (NO) release in rat intestinal arterioles during sympathetic nerve activation. To determine whether these vessels contain endothelial α2-adrenoceptors linked to thel-arginine-NO pathway, intravital microscopy was used to study the response of first-order arterioles (1As, 20–40 μm ID) to direct application of 1) the selective α2-agonist BHT-933 and 2) norepinephrine (NE) or sympathetic nerve stimulation before and after α1- or α2-receptor blockade. The effect of sympathetic nerve stimulation on 1A wall shear rate (WSR) was also determined to evaluate the possibility of hemodynamic shear stress as a stimulus for NO release. BHT-933 had no effect on 1A diameter, whereas NE produced dose-dependent constrictions of 5 ± 3 to 15 ± 3 μm, which were usually abolished by the α1-antagonist prazosin but unaffected by the α2-antagonist idazoxan. Sympathetic nerve stimulation at 3, 8, and 16 Hz induced constrictions of 4 ± 1, 8 ± 2, and 17 ± 4 μm, respectively, and these constrictions were also usually abolished by prazosin but unaffected by idazoxan. Resting WSR averaged 1,997 ± 163 s−1 and decreased to 1,587 ± 209, 1,087 ± 195, and 537 ± 99 s−1 during 3-, 8-, and 16-Hz nerve stimulation. These results suggest that α2-adrenoceptor-dependent pathways do not influence either resting tone or sympathetic constriction of proximal arterioles in the intestinal submucosa and that luminal shear stress in these vessels significantly decreases with sympathetic constriction. It therefore appears unlikely that either α2-receptor activation or changes in hemodynamic shear serve as stimuli for arteriolar NO release during periods of increased sympathetic nerve activity.

Arteriolar network response to pressure reduction during sympathetic nerve stimulation in cat skeletal muscle

1994 ◽  
Vol 266 (3) ◽  
pp. H1251-H1259 ◽  
Author(s):  
P. Ping ◽  
P. C. Johnson
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Similar Degree ◽  
Sartorius Muscle ◽  
Pressure Reduction ◽  
Third Order ◽  
Sympathetic Nerve Stimulation ◽  
Resistance Change

Previous studies in this laboratory have shown that autoregulation of blood flow and dilation of midsized (second-order) arterioles were significantly enhanced during sympathetic nerve stimulation of cat sartorius muscle apparently because of a greater myogenic response of the arterioles. Quite typically, blood flow increased with arterial pressure reduction to 80, 60, and 40 mmHg (superregulation) during sympathetic nerve stimulation. To determine the contribution of the various orders of arterioles to the enhanced autoregulation, we measured diameters in all orders of arterioles and measured red cell velocity in first-, second-, and third-order arterioles. Without sympathetic nerve stimulation, all orders of arterioles except the first order dilated to pressure reduction, but flow autoregulation was weak. With sympathetic nerve stimulation, arteriolar dilation to pressure reduction was significantly enhanced in all six orders of arterioles, and flow rose significantly. The resistance change in the arteriolar network during pressure reduction as calculated from diameter changes was greatest in third- and fourth-order arterioles. Experimentally determined flow changes to pressure reduction and to sympathetic nerve stimulation were quantitatively similar to those predicted from diameter changes in a model of the arteriolar network. Calculated wall shear stress (from viscosity and shear rate) for first-, second-, and third-order arterioles decreased during pressure reduction with and without sympathetic nerve stimulation. We concluded that endothelium-mediated dilation due to shear stress would tend to oppose autoregulation of blood flow to a similar degree under both circumstances.

Atrial natriuretic factor attenuates sympathetic neuroeffector responses in hindlimb vasculature of rabbits

1989 ◽  
Vol 67 (9) ◽  
pp. 1101-1105 ◽  
Author(s):  
K. P. Patel
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Sympathetic Nerve Stimulation ◽  
Arterial Infusion ◽  
Natriuretic Factor ◽  
Before And After ◽  
Atrial Natriuretic

To determine whether atrial natriuretic factor (ANF) affects vasoconstrictor responses to electrical stimulation of sympathetic nerves or intra-arterial norepinephrine (NE), changes in perfusion pressure were measured during lumbar sympathetic nerve stimulation (LSNS, 1–8 Hz), or administration of NE (50–200 ng), in an isolated constant flow-perfused hindlimb of chloralose-anesthetized rabbit before and after intra-arterial infusion of ANF (0.5 ng∙mL−1∙min−1). ANF significantly attenuated responses to LSNS (relative potency, RP = 0.65) and to NE (RP = 0.47). We conclude that ANF attenuates vasoconstrictor responses to both LSNS and NE. Thus ANF alters sympathetic nervous system mediated changes in vascular resistance possibly at the neuroeffector site.Key words: atrial natriuretic factor, sympathetic nerve stimulation, vasculature.

Responses of the atrial myocardium to cardiac sympathetic nerve stimulation

1985 ◽  
Vol 249 (2) ◽  
pp. H207-H211
Author(s):  
Y. Masuda ◽  
M. N. Levy
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Cardiac Tissue ◽  
Ventricular Myocardium ◽  
Neuronal Uptake ◽  
Atrial Myocardium ◽  
Uptake Mechanism ◽  
Sympathetic Nerve Stimulation ◽  
Cardiac Tissues ◽  
Before And After

The cardiac responses to sympathetic nerve stimulation were measured in open-chest, anesthetized dogs before and after infusions of cocaine, which were given to inhibit the neuronal uptake of norepinephrine. Cocaine did not augment the inotropic or chronotropic responses, but it did retard their decay after cessation of sympathetic stimulation. Before cocaine, the half-times for decay of the chronotropic, atrial inotropic, and ventricular inotropic responses were 28.4 +/- 2.2, 29.8 +/- 2.7, and 22.1 +/- 1.9 (+/- SE) s, respectively. After cocaine, however, the half-times were significantly greater (147 +/- 12.0, 51.4 +/- 3.9, and 32.9 +/- 2.5 s, respectively). The cocaine-induced prolongation of the decay time in a given cardiac tissue is a measure of the relative efficacy of neuronal uptake as a mechanism for dissipating the neurally released norepinephrine. Our data indicate, therefore, that among the various cardiac tissues that we studied, the neuronal uptake mechanism is least effective in the ventricular myocardium, somewhat more effective in the atrial myocardium, and most effective in the sinoatrial nodal region.

Interactive Effects of Verapamil and Sympathetic Nerve Stimulation on the Sinus and AV Nodes in the Canine Hearts.

1992 ◽  
Vol 33 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Katsusuke YANO ◽  
Masanobu HIRATA ◽  
Takao MITSUOKA ◽  
Yoriaki MATSUMOTO ◽  
Tetsuya HIRATA ◽  
...  
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Interactive Effects ◽  
Sympathetic Nerve Stimulation

What do antagonists tell us about α-adrenoceptors?

1985 ◽  
Vol 68 (s10) ◽  
pp. 15s-19s ◽  
Author(s):  
G. M. Drew
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Isolated Heart ◽  
Coupling Mechanism ◽  
Sympathetic Nerve Stimulation ◽  
Stimulus Response ◽  
Adrenoceptor Agonist ◽  
Tissue Responses ◽  
Cat Spleen ◽  
Relative Potencies

The early proposals that pre- and post-junctional α-adrenoceptors might be different stemmed largely from two separate observations. Firstly, the orders of potency of a series of agonists at inhibiting the response to sympathetic nerve stimulation and in increasing inotropic activity in the rabbit isolated heart were different [1, 2]. Secondly, phenoxybenzamine was more potent in inhibiting vasoconstrictor responses to sympathetic nerve stimulation than in increasing transmitter overflow from the cat spleen [3]. These experiments illustrate the most fundamental, pharmacological ways of distinguishing between receptors: namely, by comparing the relative potencies of agonists and/or antagonists in producing, or preventing, pharmacological effects. There are, however, difficulties in using agonists to classify receptors because their ability to generate a response depends not only upon their intrinsic properties of affinity for, and efficacy at, the receptors but also upon the capacity of the tissue to translate the stimulus into a response. Thus agonists with a relatively low intrinsic efficacy may produce a small response, or no response at all, in a tissue in which the efficiency of the stimulus-response coupling mechanism is low. The importance of this phenomenon in influencing tissue responses to agonists with low efficacy has been demonstrated for the α-adrenoceptor agonist prenalterol [4] and for the α-adrenoceptor agonist oxymetazoline [5].

Sign in / Sign up

Export Citation Format

Share Document